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To evaluate the nutritional consequences of acute lymphoblastic leukemia and its treatment, 15 children with leukemia were studied. Anthropometric data, fat-free mass by impedance, energy intake, and resting energy expenditure (REE) were determined at diagnosis and on days 22, 36, and 71 of the treatment. Interleukin (IL)-1 beta, IL-6, interferon-gamma, and tumor necrosis factor were also measured. Fifteen healthy control subjects were matched for age and sex. Body weight and height and body composition were comparable at all times of the study, although three children were underweight at diagnosis (weight-for-height < 85% of French standards). Although two different methods were used for dietary recall in the two groups, energy intake expressed as a percentage of normal recommended values for age and sex was lower in patients than in control subjects (104 +/- 19%) on day 1 (47 +/- 32.1%) and day 22 (58 +/- 24%), but was comparable on day 36 (85 +/- 71%) and day 71 (85 +/- 48%). This low energy intake involved both carbohydrates and fats. Energy and carbohydrate intakes improved significantly during the study in patients. The nonprotein respiratory quotient (RQ) in patients was significantly lower than in control subjects (0.84 +/- 0.04) on day 1 (0.79 +/- 0.02) but was comparable on day 71. The REE of the patients on day 1 (5057.8 +/- 1588.4 kJ/24 h) and day 71 (4844.7 +/- 116.1 kJ/24 h) and of the control subjects (4313.8 +/- 823.5 kJ/24 h) was not significantly different. Cytokines remained undetectable on days 1, 36, and 71. The results showed that at the time of diagnosis and during this period of chemotherapy there was no evidence of raised REE. The poor intakes during the first month of chemotherapy were recent as shown by the parents' questionnaire responses and the absence of consequences in body composition. The transient decrease in RQ seemed to be an adaptative mechanism to the poor carbohydrate intake. No indication of undernutrition in the patients as a group was evident during the first 71 d of treatment although further long-term nutritional assessment is needed.

The high prevalence of obesity at an early stage of Duchenne muscular dystrophy (DMD) could result not solely from reduced physical activity, but may also involve low resting energy expenditure (REE), abnormal nutrient utilization, or overfeeding. We hypothesized that the dramatic muscle mass loss in DMD should reduce the REE. REE was measured by indirect calorimetry in 13 9-13-y-old DMD boys (5 obese, 8 nonobese) and 9 male age-matched controls. Muscle mass was estimated from 3-d creatinine excretion in urine. Daily energy intake was estimated from 7-d diet records. In the nonobese DMD group (NODMD) the muscle mass was reduced by 71%, and the REE was 13% lower than in controls (47.5 versus 54.6 kcal.h-1, p < 0.05). Postabsorptive respiratory quotients appeared higher in both DMD groups than in the controls; however, the difference was significant only for the NODMD group (0.88 versus 0.83, p < 0.05). Respiratory quotients were not different between the two DMD groups. Diet records were not contributive in revealing a different dietary behavior between groups. Our results suggest that: 1) muscle mass loss in DMD is associated with a low REE, 2) low postabsorptive fat utilization might occur at an early stage of the disease, and 3) obesity is not associated with an increase in fat utilization in DMD. This study warrants further research to test low REE and low fat utilization as risk factors in developing obesity in DMD.

Once daily amikacin administration associated with ceftazidime is well tolerated for the treatment of Pseudomonas aeruginosa pulmonary exacerbations in cystic fibrosis patients. Serum peak levels and diffusion in sputum are higher than with a conventional schedule.

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